ArticleAllergy, asthma & immunology research2026
E2F1-Activated lncRNA FTX Promotes Asthma Progression via Regulating the SRSF1/RBPJ Axis.
Article in Allergy, asthma & immunology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
purposeLong non-coding RNA five prime to Xist (FTX) is considered a regulator for asthma. Therefore, we aimed to explore its more roles and molecular mechanisms in asthma process.
methodsSerum samples from controls and asthmatics were collected. Asthma mouse models were induced with ovalbumin (OVA), and cell models were established using airway smooth muscle cells (ASMCs) treated with platelet-derived growth factor BB (PDGF-BB). The inspiratory and expiratory airway resistances of mice were examined by measuring airway hyperresponsiveness. The pathological changes of mice lung tissues were observed by hematoxylin & eosin, periodic acid-Schiff, and Masson staining. Serum immunoglobulin E and inflammatory factor levels were detected using an enzyme-linked immunosorbent assay. The CCK-8, Transwell, and flow cytometry were used to assess cell function. FTX, E2F family transcription factor 1 (E2F1), serine rich/arginine splicing factor 1 (SRSF1), and recombination signal binding protein J (RBPJ) levels measured by quantitative real-time-polymerase chain reaction or Western blotting. The relationships among FTX, E2F1, SRSF1, and RBPJ were evaluated by dual-luciferase report, ChIP, RNA pull-down and RIP assay. The effect of FTX/SRSF1 on RBPJ mRNA stability was analyzed by the actinomycin D treatment assay.
resultsUpregulated FTX was detected in asthmatic patients, asthma mice, and PDGF-BB-induced ASMCs. FTX downregulation repressed PDGF-BB-induced ASMCs viability, migration, and inflammation. E2F1 bound to the FTX promoter region to activate its expression, and E2F1 downregulation could repress PDGF-BB-induced ASMCs function via reducing FTX expression. Also, FTX stabilized RBPJ mRNA by interacting with SRSF1. RBPJ overexpression reversed the downregulation effect of FTX knockdown on PDGF-BB-induced ASMCs viability, migration, and inflammation. Meanwhile, E2F1 downregulation alleviated mouse asthma symptoms by inhibiting the FTX/SRSF1/RBPJ pathway.
conclusionsFTX, transcriptionally activated by E2F1, promoted asthma progression via the the regulation of the SRSF1/RBPJ pathway, thereby providing a possible therapeutic target for asthma treatment that warrants further validation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.